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Oral erdosteine administration attenuates cisplatin-induced renal tubular damage in rats

Zeki Yildirim1, Sadik Sogut, Ersan Odaci

  • 1Department of Pulmonary, Turgut Ozal Medical Center, Inonu University School of Medicine, 44069, Malatya, Turkey. zyildirim@inonu.edu.tr

Pharmacological Research
|January 25, 2003
PubMed

Insights

Erdosteine, a free radical scavenger, protected against cisplatin-induced acute renal failure in rats by reducing kidney damage markers and oxidative stress. Further studies are needed to confirm its efficacy.

Area of Science:

  • Pharmacology
  • Toxicology
  • Nephrology

Background:

  • Cisplatin is a widely used chemotherapy agent with significant nephrotoxicity.
  • Oxidative stress plays a crucial role in cisplatin-induced kidney damage.
  • Therapeutic strategies to mitigate cisplatin nephrotoxicity are urgently needed.

Purpose of the Study:

  • To investigate the protective effects of erdosteine, a free radical scavenger, against cisplatin-induced acute renal failure in a rat model.
  • To evaluate the impact of erdosteine on oxidative stress markers and kidney function in cisplatin-treated rats.

Main Methods:

  • Acute renal failure was induced in rats using a single dose of cisplatin.
  • Rats were treated with oral erdosteine.
  • Kidney damage was assessed through histological examination.
  • Plasma creatinine and blood urea nitrogen (BUN) levels were measured.
  • Tissue levels of malondialdehyde (MDA) and nitric oxide (NO) were determined.
  • Activities of antioxidant enzymes, including catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD), were measured.

Main Results:

  • Cisplatin administration led to significant kidney damage, elevated plasma creatinine and BUN levels, and increased tissue MDA and NO.
  • Erdosteine treatment attenuated the cisplatin-induced increases in plasma creatinine and BUN.
  • Erdosteine reduced elevated tissue MDA and NO levels, indicating a decrease in oxidative stress.
  • Histological examination confirmed that erdosteine provided protection against cisplatin-induced renal damage.
  • Erdosteine treatment mitigated the depletion of antioxidant enzyme activities (CAT, GSH-Px, SOD) caused by cisplatin.

Conclusions:

  • Erdosteine demonstrates significant protective effects against cisplatin-induced nephrotoxicity in rats.
  • The renoprotective mechanism of erdosteine involves the reduction of oxidative stress and preservation of antioxidant enzyme activity.
  • Erdosteine shows promise as a therapeutic agent for preventing or treating cisplatin-induced kidney damage.
  • Further research with varying erdosteine doses is recommended to fully elucidate its therapeutic potential.

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